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Related Experiment Video

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Laquinimod ameliorates secondary brain inflammation.

Julia Nedelcu1, Christin Reinbach1, Philipp Riedler1

  • 1Institute of Anatomy, Rostock University Medical Center, Rostock 18057, Germany; Department of Anatomy II, Ludwig-Maximilians-University of Munich, Munich 80336, Germany.

Neurobiology of Disease
|November 16, 2019
PubMed
Summary

Degenerative brain processes in Multiple Sclerosis (MS) can cause inflammation. Ameliorating brain degeneration with Laquinimod reduced immune cell recruitment and inflammatory lesion development in a pre-clinical MS model.

Keywords:
CuprizoneDemyelinationLaquinimodMultiple sclerosis

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Area of Science:

  • Neuroimmunology
  • Neuroinflammation
  • Demyelinating diseases

Background:

  • Brain degeneration can initiate inflammatory lesions in Multiple Sclerosis (MS).
  • Understanding the link between primary neurodegeneration and secondary inflammation is crucial for MS treatment.
  • Novel therapeutic strategies aim to halt disease progression by targeting early degenerative events.

Purpose of the Study:

  • To investigate if mitigating primary neural degeneration reduces secondary peripheral immune cell infiltration and inflammatory lesion formation in a pre-clinical MS model.
  • To evaluate the efficacy of Laquinimod in preventing cuprizone-induced neurodegeneration and subsequent inflammatory responses.
  • To assess the impact of targeting neurodegeneration on immune cell recruitment in an experimental autoimmune encephalomyelitis (EAE) model.

Main Methods:

  • Utilized a pre-clinical MS model involving cuprizone intoxication to induce neural degeneration.
  • Administered Laquinimod during the cuprizone intoxication period to ameliorate pathology.
  • Induced experimental autoimmune encephalomyelitis (EAE) by immunization with myelin oligodendrocyte glycoprotein (MOG) peptide.
  • Assessed demyelination, axonal injury, and reactive gliosis via immunohistochemistry.
  • Employed Positron Emission Tomography (PET) imaging to analyze in vivo glia activation.

Main Results:

  • Vehicle-treated mice showed extensive demyelination, glia activation, and enhanced TSPO-ligand binding.
  • Laquinimod treatment significantly ameliorated cuprizone-induced pathology, including demyelination and glia activation.
  • In the Cup/EAE model, cuprizone-induced pathology triggered substantial peripheral immune cell recruitment into the brain.
  • Laquinimod treatment reduced this secondary immune cell recruitment without altering the primary anti-MOG immune response.
  • Neuro-axonal injury and multifocal perivascular inflammation were observed in vehicle-treated Cup/EAE mice.

Conclusions:

  • Amelioration of primary brain-intrinsic degenerative processes can halt secondary peripheral immune cell recruitment.
  • Targeting neurodegeneration offers a promising therapeutic strategy to prevent inflammatory lesion development in MS.
  • These findings have significant implications for interpreting clinical trial results and developing new MS therapies.